3.2 LTR Retrotransposons (pg 287): Human LTR retrotransposons are retrovirus-like elements retro-transposed in the genome and inherited by the host from generation to generation. It is believed that human LTR retrotransposons are descendants of exogenous retroviruses that repeatedly infected germlines of human ancestors and became endogenous. Endogenous retroviruses retain their ability to retrotranspose within cells for some time, but cannot be transmitted efficiently between cells. But see trojan exosome hypothesis(hiv researchers) and reinfection PNAS paper. Their subsequent evolution reflects adaptation to an intracellular environment, simplification, and formation of non-autonomous copies.

Most HERVs are extinct and are represented only by mutated interspersed copies, particularly by LTRs. Analogous to birds representing the extinct dinosaurs. The interspersed copies of the LTR retrotransposons constitute around 9% of the human genome. Although LTR retrotransposons are not as abundant as the non-LTR retrotransposons, they are by far the most diverse and complex TEs harbored by our genome. Approximately 200 families of LTR retrotransposons have been identified in the human genome. A vast majority of them were identified and reconstructed using computer-assisted sequence analysis.

On the basis of similarities to known animal exogenous retroviruses, all LTR retrotransposons present in the human genome can be divided into three classes (Table 3):

Historically, LTR retrotransposons were viewed as “retroviral-like” except they “did not encode env protein. Currently they are considered as non-autonomous retrovirus derived elements and the originally introduced distinction between retroviruses and LTR retrotransposons is becoming obsolete.”

Vectors: viruses, gametes, organisms, plasmids or other agents that can deliver genes by HGT.

HGT may be defined as any occurrence of heritable material passing between organisms, asynchronous with reproduction of organisms. It represents replication of heritable material outside the context of parent to offspring (i.e. vertical) reproduction. Three types of evidence traditionally lead to claims of HGT. First, biochemical and genetic observations of real time (usually recreations of) gene flow between two genotypically distinguishable individuals. Secondly, DNA sequences that are common within a species but inconsistently found in that genus, and finally direct evidence of processes that can create genes that reproduce horizontally. HGT is now confirmed to occur between all biological kingdoms and has consequences even when genes fail to introgress.

It (HGT) “has been packaged into separate boxes that go by other names”.

Viruses and Transduction (pg 343) – “Transduction is distinctive because like transformation, it delivers genes most recently of chromosomal origin that become stably integrated into the recipient genome.”

Here’s a version of what I was writing about on the stolen virus issue.

It’s edited for removal of the personal.

One should bother to read the entire Crewdson file to not miss the significance of Monti’s LAI, which had contaminated his “LAV” culture. Also, the entire Crewdson file reveals all the funny business on Monti’s end. He didn’t just have one “isolate”, for example. Insitute Pasteur had “nothing” in Gallo’s terms because they had only figured out “primary isolates”. Only Popovic was capable of “growing LAV” in continuous production culture in 1984, which they didn’t realize was actually LAI until 1991.

“It was conclusive proof that the French virus was secretly used”.

So secret that Popovic labels their special HUT 78 cell line for “growing viruses”, “HUT 78/LAV”.

Here’s a quote from Gallo’s letter to Nature; admitting why the RT activity and “HTLV” protein expression in his “natural isolates” was so goosed up:

“It also appears that cultures of virus from people with AIDS became contaminated with HIV-LAI at NIH. When workers at the Institute Pasteur and at NIH later cloned viruses from AIDS patients, both apparently sequenced LAI. At the Institute Pasteur, this virus was designated LAV-BRU. At NIH this virus was designated HTLV – IIIB.” (Nature, V351, 30 May 1991, 358)

What I had put up for all dissidents to read well before JR/Crowe project was from a later Nature paper by investigators from OSI* confirming Gallo’s account. It concluded that indeed, the primary culture from patient BRU, a supposed “natural isolate” – the “first HIV” – later the basis of Nobel Prize – was “contaminated” by culture derived from patient LAI.

*Office of Scientific Integrity and precisely analyzed by Nature, V363 (3 June 1993), 466-469: the “contaminated culture (M2T-/B was sent to LTCB (Gallo’s lab) in September 1983”. This paper also reveals the reason for the “provenance” of LAV in this culture, “the contamination of a culture derived from patient BRU by one from patient LAI was responsible for the provenance of LAV*.”

Two points of evidence for recombination in the H9 culture between the 3 prime half of LAV with LTR gag-pol of HTLV is

1) the “similarity” of HTLV III/LAV with “Montagmier’s virus” was detemined with measurements of the “env V1/V2 region” and

2) “We conclude that the pool (HT), and probably another LTCB culture, MoV, were contaminated between October 1983 and early 1984 by variants of LAV from the M2T-/B culture.”

(There’s more besides these two points.) H9 and H4, of course, were derived from HT pool. One can say that Popovich/Gallo “massaged” (words fail here) Montagnier’s “isolate” in a manner not unlike the “isolates” from those 48 patients.

I think it was Lanka who said a “witches brew” was the basis of “HIV isolation.”

Gene

Summarizing my long responses: HERVs in genome of special cell-cultures used 1980 to 1986 would predictably produce retrovirally coded poly A RNA based on knowledge obtained from ten years (1970-1980) of NIH Cancer Program research of Gallo et al. By 1980, they knew how to design “immortal cells” that would produce recombined poly A RNA originating from retroviral genomic DNA and “fish it out” of culture supernatants. It would appear to be exogenous; i.e. they knew the cDNA from the “special” poly A RNA would not match up to the chromosomal DNA (genetic engineering: inducing RNA “editing” enzymes, recombination, etc.).